As a result of previous experimental studies, we have proposed the concept that gastric ulcers are usually caused by a hypersecretion of gastric juice of gastrin origin brought about by stasis of food in the stomach as a result of pyloric stenosis or gastric atony. This view has been challenged and the suggestion has been made that gastric ulcers are not acid-peptic in origin, but are caused by regurgitation of bile and pancreatic juice into the stomach. To test this theory we have diverted bile and pancreatic juice into the stomach and esophagus of dogs by a modified Mann-Williamson procedure. This diversion did not produce ulcers in the esophagus or stomach in seven months. We have confirmed the observations of Claude Bernard tht the legs of living frogs introduced into the stomach of the dog are digested away by the dog's gastric content. Legs of living frogs introduced into the duodenum and exposed to the digestant action of bile, pancreatic juice and intestinal juice are not digested away if the gastric juice is diverted away from the duodenum. Similarly, the leas of living frogs introduced into the jejunum are not digested away. The implantation of the spleen into the fundus of the gallbladder did not cause progressive necrosis of the spleen. We have recently succeeded in preparing dogs each with two vagus innervated isolated pouches of the fundus of the stomach. These pouches have responded to insulin glycemia indicating that the vagus nerves to each pouch are intact. We propose to use this preparation in a further study of the physiology of the afferent fibers in the vagus nerves. We wish to test the influence of these afferent fibers on gastric secretion and to determine whether or no they play a role in the regulation of the secretion of gastric juice. It is hoped that this will throw light on the pathogenesis of gastric ulcers.